PURSE 2004
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Browsing PURSE 2004 by Author "Adikaram, N. K. B."
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- ItemCanker Disease of Psidium Guajava L. Caused by Pestalotiopsis Psidii and Host Defencive Responses(University of Peradeniya, 2004-11-10) Bandaranayake, B. M. R. P.; Adikaram, N. K. B.Canker disease caused by Pestalotiopsis psidii in unripe guava is characterized by browning and cracking of outermost epicarp. Cracking exposes the internal tissues of fruits resulting secondary infections. Infection and development of limited symptoms occur in the field and may develop into progressive fruit rot during ripening. It does not penetrate deeply but reduces the market value. When fruits are severely infected, mummified fruits fall off resulting in yield losses. Causative agent was isolated from the infected areas as well as from healthy internal tissues where symptoms were not visible. The fungus may therefore exist as an endophyte. Healthy and canker infected epicarp tissues of mature and immature fruits were extracted in ethyl acetate for antifungal zones. Four pre-formed antifungal zones were detected on TLC bioassay in healthy tissues. Only two antifungal zones were present in TLC, which was extracted from infected tissues. No additional or larger antifungal zones were present in the extracts taken from infected tissues. Infected tissues observed were yellowish brown in colour and the cells had disintegrated. The infected necrotic tissues did not show deposition of lignin, suberin or tannins. Measurement of pH at the canker infected and healthy areas of the guava fruits, did not show a significant difference. These investigations have revealed that the primary defense response in guava fruit against the canker pathogen brings about rapid necrosis development in which no phytoalaexins were accumulated.
- ItemChanges in pH Following Freckle Infection (Phyllosticta Musarum) as a Defense Response Against Anthracnose(University of Peradeniya, 2004-11-10) Weerakoon, A. U.; Adikaram, N. K. B.; Abeysekara, C. L.The host environment pH is found to be a regulatory factor in pathogenesis of certain fungi. Some fungi increase the host pH while others tend to reduce it. Certain ColLetotrichum spp. have the ability to modulate host pH by secreting ammonia locally into the host tissue, resulting in a pH increase which enables enzymatic secretion and enhance virulence. Colletotrichum musae causes quiescent infections in unripe green banana fruits which develop into anthracnose lesions during fruit ripening. Freckle disease in banana caused by Phyllosticta musarum is associated with a number of defence responses viz. accumulation of phytoalexin and PR proteins, and certain other changes such as lignification and suberization and accumulation of tannins, which in turn reduce the development of anthracnose disease. Six phytoalexins have been isolated from freckle infected banana peel, which contribute to defense against C. musae. The objective of this study was to determine whether P. musarum causes a pH alteration in the banana peel and if so whether this acts as an additional defence response by the fungus against anthracnose. Freckled and non freckled "Embul'' fruits at a similar stage of maturity were obtained from the same bunch. A set of freckled fruits and non freckled fruits were inoculated with 50 III of C. musae spore suspension (105 spores ml") per inoculation, while the control sets of freckled and non freckled fruits were treated with sterile distilled water. Lesion diameters and pH of the peel were measured daily for 7 days. There was a significantly higher anthracnose development in non freckled fruits compared to the freckled fruits. This was observed when fruits were artificially inoculated and also when natural quiescent infections of C. musae were allowed to develop. The freckle infected banana peel had a significantly (p=O.05 level) higher pH than the non freckled peel throughout the ripening process. This indicates that P. musarum infection increases host pH. In fruits inoculated with C. musae, the peel pH was significantly higher (p = 0.05 level) in the freckled peel compared to the non-freckled peel during initial necrosis. Furthermore, at the onset of tissue maceration pH of the freckled peel was higher than that of the non-freckled peel. However with the expansion of lesions the pH in the non-freckled peel was significantly higher at p=0.05 level, when compared to the freckled peel. The higher values of pH in the freckled peel during initial necrosis and the onset of tissue maceration could be a contributing factor in limiting anthracnose in bananas. The increase in pH at an advanced stage of lesion development, in non freckled peel, may be due to rapid tissue maceration caused by C. musae. These results indicate that pH increase following P. musarum infection may be an additional defense response in banana fruit.